Causes of Lung Failure

Many types of lung injury can result from medications, and it is often impossible to predict who will develop lung disease resulting from a medication or drug.

The types of lung diseases that may result from medications include:

• Allergic reactions -- asthma, hypersensitivity pneumonitis, or eosinophilic pneumonia
• Alveolar hemorrhage, which is bleeding into the lung air sacks
• Bronchitis
• Drug-induced lupus erythematosus
• Granulomatous lung disease -- a type of tumor in the lungs
• Inflammation of the lung air sacks (pneumonitis or infiltration)
• Interstitial fibrosis
• Lung failure
• Lung vasculitis, which is inflammation of lung blood vessels
• Mediastinitis
• Pulmonary edema
• Pleural effusion
• Swollen lymph nodes

Many drugs are known to cause lung disease in some people, including those used during chemotherapy and to treat certain heart conditions. Other drugs known to cause lung disease in some people include certain antibiotics and illicit drugs.

Symptoms of Lung Failure

Bloody sputum
Chest pain
Cough
Fever
Shortness of breath
Wheezing
Note: Symptoms may vary from person to person.

Exams and Tests of Lung Failure

The doctor will perform a physical exam and listen to your chest and lungs with a stethoscope. Abnormal breath sounds may be heard.

Tests that may be done include:

• Bronchoscopy
• Complete blood count with blood differential
• Chest CT scan
• Chest x-ray
• Lung biopsy (in rare cases)
• Thoracentesis (if pleural effusion is present)

Treatment of Lung Failure

The first step is to stop using the prescription drug causing the problem. Other treatments depend on your specific symptoms. For instance, you may need oxygen until the drug-induced lung disease improves. Powerful anti-inflammatory medicines called steroids are sometimes used and may quickly reverse the lung inflammation.

Outlook / Prognosis of Lung Failure

Acute episodes usually go away within 48 - 72 hours after the medication has been discontinued, but chronic syndromes may take longer to resolve. Some drug-induced lung diseases such as pulmonary fibrosis may never go away.

Possible Complications of Lung Failure

Diffuse interstitial pulmonary fibrosis
Hypoxemia (low blood oxygen)
Respiratory failure

When to Contact a Medical Professional

Call your health care provider if you develop symptoms of this disorder.

Prevention of Lung Failure

Any previous reaction to a medication should be noted, so that you can avoid the medication in the future. Wear a medical allergy bracelet if you have known drug reactions. Avoid the abuse of illicit drugs, as this will prevent many drug-induced lung diseases.

Pleural effusion is a cause of lung failure

A pleural effusion is an accumulation of fluid between the layers of tissue that line the lungs and chest cavity.

Causes of Lung Failure

Your body produces pleural fluid in small amounts to lubricate the surfaces of the pleura, the thin tissue that lines the chest cavity and surrounds the lungs. A pleural effusion is an abnormal, excessive collection of this fluid.

Two different types of effusions can develop:

1. Transudative pleural effusions are caused by fluid leaking into the pleural space. This is caused by elevated pressure in, or low protein content in, the blood vessels. Congestive heart failure is the most common cause.
   
   
2. Exudative effusions usually result from leaky blood vessels caused by inflammation (irritation and swelling) of the pleura. This is often caused by lung disease. Examples include lung cancer, lung infections such as tuberculosis and pneumonia, drug reactions, and asbestosis.

Symptoms of Lung Failure

• Chest pain, usually a sharp pain that is worse with cough or deep breaths
• Cough
• Fever
• Hiccups
• Rapid breathing
• Shortness of breath
• Sometimes there are no symptoms.

Exams and Tests of Lung Failure

During a physical examination, the doctor will listen to the sound of your breathing with a stethoscope and may tap on your chest to listen for dullness.

The following tests may help to confirm a diagnosis:

• Chest x-ray
• Pleural fluid analysis (examining the fluid under a microscope to look for bacteria, amount of protein, and presence of cancerous cells)
• Thoracentesis (a sample of fluid is removed with a needle inserted between the ribs)
• Thoracic CT
• Ultrasound of the chest

Treatment of Lung Failure

Treatment may be directed at removing the fluid, preventing it from accumulating again, or addressing the underlying cause of the fluid buildup.

Therapeutic thoracentesis may be done if the fluid collection is large and causing pressure, shortness of breath, or other breathing problems, such as low oxygen levels. Removing the fluid allows the lung to expand, making breathing easier. Treating the underlying cause of the effusion then becomes the goal.

For example, pleural effusions caused by congestive heart failure are treated with diuretics (water pills) and other medications that treat heart failure. Pleural effusions caused by infection are treated with appropriate antibiotics. In people with cancer or infections, the effusion is often treated by using a chest tube for several days to drain the fluid. Chemotherapy, radiation therapy, surgery, or instilling medication into the chest that prevents re-accumulation of fluid after drainage may be used in some cases.

Outlook/Prognosis of Lung Failure

The expected outcome depends upon the underlying disease.

Possible Complications

A lung surrounded by excess fluid for a long time may collapse.
Pleural fluid that becomes infected may turn into an abscess, called an empyema, which requires prolonged drainage with a chest tube placed into the fluid.
Pneumothorax (air within the chest cavity) can be a complication of the thoracentesis procedure.

When to Contact a Medical Professional

Call your health care provider if you have symptoms of pleural effusion.

Call your provider or go to the emergency room if shortness of breath or difficulty breathing occurs immediately after thoracentesis.

Black Lung Disease

In the last decade, over 10,000 miners have died of coal workers' pneumoconiosis, or what is commonly called black lung disease.

Black lung disease, which is caused by inhaling coal mine dust, results in scarring of the lungs and emphysema, shortness of breath, disability, and premature death. While the prevalence of black lung disease had decreased by about 90% from 1969 to 1995 following the enactment of the Coal Mine Health and Safety Act, the downward trend of this disease in coal miners has stopped. Since 1995, the prevalence of black lung cases has more than doubled.

Many current underground miners (some as young as in their 30s) are developing severe and advanced cases. Identification of advanced cases among miners under age 50 is of particular concern, as they were exposed to coal-mine dust in the years after implementation of the disease prevention measures mandated by the 1969 federal legislation. An increased risk of pneumoconiosis has also been associated with work in certain mining jobs, in smaller mines, in several geographic areas, and among contract miners.

While the exact causes for the continued occurrence of black lung disease are not fully understood, possible explanations include:

1. inadequacies in the mandated coal-mine-dust regulations
2. failure to comply with or adequately enforce those regulations
3. lack of disease prevention measures to accommodate changes in mining practices (e.g., thin-seam mining with cutting of adjacent silica-containing rock) brought about by depletion of richer coal reserves
4. the effect of working longer hours in recent years, and
5. missed opportunities by miners to be screened for early disease and take action to reduce dust exposure

To help recognize early disease in miners and to enable those with black lung to take action to reduce their dust exposures, NIOSH operates the Coal Workers' Health Surveillance Program. Miners who participate in the program receive no cost health evaluations (including a chest x-ray) once every five years. Chest x-rays can detect the early signs of coal workers' pneumoconiosis and can detect lung changes often before the miner is aware of any breathing problems. These programs are meant to protect the health of the miners, but they can only do so if the miners participate. Interviews with miners have indicated that reasons for nonparticipation are manifold, including concerns that a positive finding might be disclosed to their employers and lead to job loss or affect future receipt of compensation for disability. However, under federal law a mine operator can not legally dismiss a miner due to presence of black lung disease (or any other type of disease).

Coal operators are required under the law to adhere to the dust standards. Today's mining industry has the necessary tools to control each miner's exposure to respirable dust and silica. The industry and the miners must both ensure that control measures are conscientiously applied and dust levels accurately monitored. In addition, miners need to reduce their exposure to coal-mine dust when early disease is seen and, when necessary, to exercise their legal right for transfer to a job with reduced exposure, if available. When all of this is achieved we will be one step closer to a time when miners and their families will no longer have to suffer the devastating effects of black lung disease

Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are syndromes of acute respiratory failure that result from acute pulmonary edema and inflammation. The development of ALI/ARDS is associated with several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorders such as acute pancreatitis and drug overdose. Although mortality from ALI/ARDS has decreased in the last decade, it remains high. Despite two major advances in treatment, low VT ventilation for ALI/ARDS and activated protein C for severe sepsis (the leading cause of ALI/ARDS), additional research is needed to develop specific treatments and improve understanding of the pathogenesis of these syndromes. The NHLBI convened a working group to develop specific recommendations for future ALI/ARDS research. Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI. Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.

Acute lung injury (ALI) and the acute respiratory distress syndrome(ARDS) are syndromes with a spectrum of increasing severity of lung injury defined by physiologic and radiographic criteria in which widespread damage to cells and structures of the alveolar capillary membrane occurs within hours to days of a predisposing insult. In this report we will consider ALI and ARDS together, although we also specically refer to ARDS because it has been studied as a defined entity with exclusion of patients with less severe degrees of lung injury. The time course of ALI/ARDS distinguishes these syndromes of alveolar damage from most other lung diseases, whose natural histories occur over a much longer duration, usually years. ALI/ARDS is a major cause of acute respiratory failure with high morbidity and mortality in critically ill patients.

Recent epidemiologic data indicate that the incidence of ARDS defined by consensus physiologic criteria may account for 36,000 deaths per year in a country the size of the U.S.

There is reason to believe that this number will increase significantly in the future because of increasing frequency of some predisposing conditions that precipitate ALI/ARDS, such as sepsis.

Although there is evidence that mortality in patients with ALI/ARDS may have declined over the last 10 to 15 years, it remains high (30-40%), and it is an important cause of pulmonary and nonpulmonary morbidity in patients who leave the hospital . Until recently, there were no specific measures that altered mortality in ALI/ARDS, and management was exclusively expectant and supportive, reflecting major deficiencies in our understanding of the cellular and molecular nature, pathogenesis, and natural history of acute alveolar injury. Recently, however, a prospective multicenter clinical trial demonstrated that a lung-protective ventilatory strategy could substantially reduce mortality. The results of this clinical trial suggest that there are additional opportunities to improve outcomes in ALI/ARDS if we can increase our fund of knowledge at the basic, translational, and clinical levels.

ALI/ARDS is a cause of acute respiratory failure that develops in patients of all ages from a variety of clinical disorders, including sepsis (pulmonary and nonpulmonary), pneumonia (bacterial, viral, and fungal), aspiration of gastric and oropharyngeal contents, major trauma, and several other clinical disorders including severe acute pancreatitis, drug over dose,and blood products. Most patients require assisted ventilation with positive pressure. The primary physiologic abnormalities are severe arterial hypoxemia as well as a marked increase in minute ventilation secondary to a sharp increase in pulmonary dead space fraction. Patients with ALI/ARDS develop protein-rich pulmonary edema resulting from exudation of fluid into the interstitial and airspace compartments of the lung secondary to increased permeability of the barrier. Additional pathologic changes indicate that the mechanisms involved in lung edema are complex and that edema is only one of the pathophysiologic events in ALI/ARDS. One physiologic consequence is a significant decrease in lung compliance that results in an increased work of breathing, one of the reasons why assisted ventilation is required to support most lung-failure patients.